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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 吳益群(Yi-Chun Wu) | |
| dc.contributor.author | Chieh-Hsiang Tan | en |
| dc.contributor.author | 譚傑祥 | zh_TW |
| dc.date.accessioned | 2021-06-08T04:14:04Z | - |
| dc.date.copyright | 2010-08-17 | |
| dc.date.issued | 2010 | |
| dc.date.submitted | 2010-08-13 | |
| dc.identifier.citation | Brenner, S. (1974). 'The genetics of Caenorhabditis elegans.' Genetics 77(1): 71-94.
Broverman, S. A. and P. M. Meneely (1994). 'Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans.' Genetics 136(1): 119-127. Brugnera, E., L. Haney, et al. (2002). 'Unconventional Rac-GEF activity is mediated through the Dock180-ELMO complex.' Nat Cell Biol 4(8): 574-582. Cabello, J., L. J. Neukomm, et al. (2010). 'The Wnt pathway controls cell death engulfment, spindle orientation, and migration through CED-10/Rac.' PLoS Biol 8(2): e1000297. Cho, C.-Y. (2009). Functional Study of dpy-24 and its Heterochronic REgulation in Distal Tip Cell Migration in Caenorhabditis elegans. Institute of Molecular and cellular Biology. Taipei, National Taiwan University. Master. Chung, S., T. L. Gumienny, et al. (2000). 'A common set of engulfment genes mediates removal of both apoptotic and necrotic cell corpses in C. elegans.' Nat Cell Biol 2(12): 931-937. Conradt, B. and H. R. Horvitz (1998). 'The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9.' Cell 93(4): 519-529. Conradt, B. and H. R. Horvitz (1999). 'The TRA-1A sex determination protein of C. elegans regulates sexually dimorphic cell deaths by repressing the egl-1 cell death activator gene.' Cell 98(3): 317-327. Cordes, S. N. (2006). Genes That Regulate Asymmetric Neuroblast Divisions in C.elegans, University of Califoria, Berkeley. Doctor of Philosophy. Danial, N. N. and S. J. Korsmeyer (2004). 'Cell death: critical control points.' Cell 116(2): 205-219. deBakker, C. D., L. B. Haney, et al. (2004). 'Phagocytosis of apoptotic cells is regulated by a UNC-73/TRIO-MIG-2/RhoG signaling module and armadillo repeats of CED-12/ELMO.' Curr Biol 14(24): 2208-2216. del Peso, L., V. M. Gonzalez, et al. (1998). 'Caenorhabditis elegans EGL-1 disrupts the interaction of CED-9 with CED-4 and promotes CED-3 activation.' J Biol Chem 273(50): 33495-33500. Demon, D., P. Van Damme, et al. (2009). 'Caspase substrates: easily caught in deep waters?' Trends Biotechnol 27(12): 680-688. Ellis, R. E. and H. R. Horvitz (1991). 'Two C. elegans genes control the programmed deaths of specific cells in the pharynx.' Development 112(2): 591-603. Ellis, R. E., D. M. Jacobson, et al. (1991). 'Genes required for the engulfment of cell corpses during programmed cell death in Caenorhabditis elegans.' Genetics 129(1): 79-94. Fielenbach, N., D. Guardavaccaro, et al. (2007). 'DRE-1: an evolutionarily conserved F box protein that regulates C. elegans developmental age.' Dev Cell 12(3): 443-455. Gumienny, T. L., E. Brugnera, et al. (2001). 'CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration.' Cell 107(1): 27-41. Gumienny, T. L., E. Lambie, et al. (1999). 'Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline.' Development 126(5): 1011-1022. Hao, J. C., T. W. Yu, et al. (2001). 'C. elegans slit acts in midline, dorsal-ventral, and anterior-posterior guidance via the SAX-3/Robo receptor.' Neuron 32(1): 25-38. Hatzold, J. and B. Conradt (2008). 'Control of apoptosis by asymmetric cell division.' PLoS Biol 6(4): e84. Hedgecock, E. M., J. E. Sulston, et al. (1983). 'Mutations affecting programmed cell deaths in the nematode Caenorhabditis elegans.' Science 220(4603): 1277-1279. Hengartner, M. O., R. E. Ellis, et al. (1992). 'Caenorhabditis elegans gene ced-9 protects cells from programmed cell death.' Nature 356(6369): 494-499. Hengartner, M. O. and H. R. Horvitz (1994). 'C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2.' Cell 76(4): 665-676. Hodgkin, J. and T. Doniach (1997). 'Natural variation and copulatory plug formation in Caenorhabditis elegans.' Genetics 146(1): 149-164. Hoeppner, D. J., M. O. Hengartner, et al. (2001). 'Engulfment genes cooperate with ced-3 to promote cell death in Caenorhabditis elegans.' Nature 412(6843): 202-206. Hsu, T. Y. and Y. C. Wu (2010). 'Engulfment of apoptotic cells in C. elegans is mediated by integrin alpha/SRC signaling.' Curr Biol 20(6): 477-486. Huang, T.-F. (2009). Caenorhabditis elegans dpy-24 integrates the temporal and spatial signals to control DTC migration. Institute of Molecular and cellular Biology. Taipei, National Taiwan University. Doctor of Philosophy. Hurwitz, M. E., P. J. Vanderzalm, et al. (2009). 'Abl kinase inhibits the engulfment of apoptotic [corrected] cells in Caenorhabditis elegans.' PLoS Biol 7(4): e99. Kamath, R. S., M. Martinez-Campos, et al. (2001). 'Effectiveness of specific RNA-mediated interference through ingested double-stranded RNA in Caenorhabditis elegans.' Genome Biol 2(1): RESEARCH0002. Kinchen, J. M., J. Cabello, et al. (2005). 'Two pathways converge at CED-10 to mediate actin rearrangement and corpse removal in C. elegans.' Nature 434(7029): 93-99. Koch, R., H. G. van Luenen, et al. (2000). 'Single nucleotide polymorphisms in wild isolates of Caenorhabditis elegans.' Genome Res 10(11): 1690-1696. Lettre, G. and M. O. Hengartner (2006). 'Developmental apoptosis in C. elegans: a complex CEDnario.' Nat Rev Mol Cell Biol 7(2): 97-108. Liu, H., T. J. Strauss, et al. (2006). 'Direct regulation of egl-1 and of programmed cell death by the Hox protein MAB-5 and by CEH-20, a C. elegans homolog of Pbx1.' Development 133(4): 641-650. Liu, Q. and Z. Paroo (2010). 'Molecular biology. Dicer's cut and switch.' Science 328(5976): 314-315. Liu, Q. A. and M. O. Hengartner (1998). 'Candidate adaptor protein CED-6 promotes the engulfment of apoptotic cells in C. elegans.' Cell 93(6): 961-972. Maurer, C. W., M. Chiorazzi, et al. (2007). 'Timing of the onset of a developmental cell death is controlled by transcriptional induction of the C. elegans ced-3 caspase-encoding gene.' Development 134(7): 1357-1368. Metzstein, M. M., M. O. Hengartner, et al. (1996). 'Transcriptional regulator of programmed cell death encoded by Caenorhabditis elegans gene ces-2.' Nature 382(6591): 545-547. Metzstein, M. M., G. M. Stanfield, et al. (1998). 'Genetics of programmed cell death in C. elegans: past, present and future.' Trends Genet 14(10): 410-416. Michael Chiorazzi, C. M., Shai Shaham (2009). The non-canonical cell death program governing tail-spike cell death requires the F box protein DRE-1. 17th International C.elegans Meeting. University of California at Los Angeles. Nakagawa, A., Y. Shi, et al. (2010). 'Caspase-dependent conversion of Dicer ribonuclease into a death-promoting deoxyribonuclease.' Science 328(5976): 327-334. Nehme, R. and B. Conradt (2008). 'egl-1: a key activator of apoptotic cell death in C. elegans.' Oncogene 27 Suppl 1: S30-40. Nehme, R., P. Grote, et al. (2010). 'Transcriptional upregulation of both egl-1 BH3-only and ced-3 caspase is required for the death of the male-specific CEM neurons.' Cell Death Differ. Parrish, J., L. Li, et al. (2001). 'Mitochondrial endonuclease G is important for apoptosis in C. elegans.' Nature 412(6842): 90-94. Parrish, J. Z. and D. Xue (2003). 'Functional genomic analysis of apoptotic DNA degradation in C. elegans.' Mol Cell 11(4): 987-996. Parrish, J. Z., C. Yang, et al. (2003). 'CRN-1, a Caenorhabditis elegans FEN-1 homologue, cooperates with CPS-6/EndoG to promote apoptotic DNA degradation.' EMBO J 22(13): 3451-3460. Peden, E., D. J. Killian, et al. (2008). 'Cell death specification in C. elegans.' Cell Cycle 7(16): 2479-2484. Peden, E., E. Kimberly, et al. (2007). 'Control of sex-specific apoptosis in C. elegans by the BarH homeodomain protein CEH-30 and the transcriptional repressor UNC-37/Groucho.' Genes Dev 21(23): 3195-3207. Reddien, P. W., S. Cameron, et al. (2001). 'Phagocytosis promotes programmed cell death in C. elegans.' Nature 412(6843): 198-202. Reddien, P. W. and H. R. Horvitz (2000). 'CED-2/CrkII and CED-10/Rac control phagocytosis and cell migration in Caenorhabditis elegans.' Nat Cell Biol 2(3): 131-136. Reddien, P. W. and H. R. Horvitz (2004). 'The engulfment process of programmed cell death in Caenorhabditis elegans.' Annu Rev Cell Dev Biol 20: 193-221. Shaham, S., P. W. Reddien, et al. (1999). 'Mutational analysis of the Caenorhabditis elegans cell-death gene ced-3.' Genetics 153(4): 1655-1671. Stanfield, G. M. and H. R. Horvitz (2000). 'The ced-8 gene controls the timing of programmed cell deaths in C. elegans.' Mol Cell 5(3): 423-433. Steller, H. (1995). 'Mechanisms and genes of cellular suicide.' Science 267(5203): 1445-1449. Sulston, J. E. and H. R. Horvitz (1977). 'Post-embryonic cell lineages of the nematode, Caenorhabditis elegans.' Dev Biol 56(1): 110-156. Sulston, J. E., E. Schierenberg, et al. (1983). 'The embryonic cell lineage of the nematode Caenorhabditis elegans.' Dev Biol 100(1): 64-119. Taylor, R. C., G. Brumatti, et al. (2007). 'Establishing a blueprint for CED-3-dependent killing through identification of multiple substrates for this protease.' J Biol Chem 282(20): 15011-15021. Thellmann, M., J. Hatzold, et al. (2003). 'The Snail-like CES-1 protein of C. elegans can block the expression of the BH3-only cell-death activator gene egl-1 by antagonizing the function of bHLH proteins.' Development 130(17): 4057-4071. Timmons, L., D. L. Court, et al. (2001). 'Ingestion of bacterially expressed dsRNAs can produce specific and potent genetic interference in Caenorhabditis elegans.' Gene 263(1-2): 103-112. Vaux, D. L. and S. J. Korsmeyer (1999). 'Cell death in development.' Cell 96(2): 245-254. Wang, X., W. Li, et al. (2010). 'Caenorhabditis elegans transthyretin-like protein TTR-52 mediates recognition of apoptotic cells by the CED-1 phagocyte receptor.' Nat Cell Biol. Wang, X., Y. C. Wu, et al. (2003). 'Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12.' Science 302(5650): 1563-1566. Wang, X., C. Yang, et al. (2002). 'Mechanisms of AIF-mediated apoptotic DNA degradation in Caenorhabditis elegans.' Science 298(5598): 1587-1592. Wicks, S. R., R. T. Yeh, et al. (2001). 'Rapid gene mapping in Caenorhabditis elegans using a high density polymorphism map.' Nat Genet 28(2): 160-164. Williams, B. W. (1988). Introduction to C.elegans Biology. The Nematode Caenorhabditis elegans New York, Cold Spring Harbor Laboratory Press: 1-16. Wu, Y. C. and H. R. Horvitz (1998). 'The C. elegans cell corpse engulfment gene ced-7 encodes a protein similar to ABC transporters.' Cell 93(6): 951-960. Wu, Y. C. and H. R. Horvitz (1998). 'C. elegans phagocytosis and cell-migration protein CED-5 is similar to human DOCK180.' Nature 392(6675): 501-504. Wu, Y. C., G. M. Stanfield, et al. (2000). 'NUC-1, a caenorhabditis elegans DNase II homolog, functions in an intermediate step of DNA degradation during apoptosis.' Genes Dev 14(5): 536-548. Wu, Y. C., M. C. Tsai, et al. (2001). 'C. elegans CED-12 acts in the conserved crkII/DOCK180/Rac pathway to control cell migration and cell corpse engulfment.' Dev Cell 1(4): 491-502. Yang, X., H. Y. Chang, et al. (1998). 'Essential role of CED-4 oligomerization in CED-3 activation and apoptosis.' Science 281(5381): 1355-1357. Yu, X., N. Lu, et al. (2008). 'Phagocytic receptor CED-1 initiates a signaling pathway for degrading engulfed apoptotic cells.' PLoS Biol 6(3): e61. Yu, X., S. Odera, et al. (2006). 'C. elegans Dynamin mediates the signaling of phagocytic receptor CED-1 for the engulfment and degradation of apoptotic cells.' Dev Cell 10(6): 743-757. Yuan, J. and H. R. Horvitz (1992). 'The Caenorhabditis elegans cell death gene ced-4 encodes a novel protein and is expressed during the period of extensive programmed cell death.' Development 116(2): 309-320. Yuan, J., S. Shaham, et al. (1993). 'The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme.' Cell 75(4): 641-652. Zhou, Z., E. Caron, et al. (2001). 'The C. elegans PH domain protein CED-12 regulates cytoskeletal reorganization via a Rho/Rac GTPase signaling pathway.' Dev Cell 1(4): 477-489. Zhou, Z., E. Hartwieg, et al. (2001). 'CED-1 is a transmembrane receptor that mediates cell corpse engulfment in C. elegans.' Cell 104(1): 43-56. Zou, H., W. J. Henzel, et al. (1997). 'Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3.' Cell 90(3): 405-413. Zou, W., Q. Lu, et al. (2009). 'Caenorhabditis elegans myotubularin MTM-1 negatively regulates the engulfment of apoptotic cells.' PLoS Genet 5(10): e1000679. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/22228 | - |
| dc.description.abstract | 細胞凋亡（apoptosis）是大部分多細胞動物在發育及維持生理平衡上所不可或缺的一種機制。在線蟲（Caenorhabditis elegans）先前的研究中已發現超過20個與此機制相關的基因，其中4個基因：egl-1(BH3-only), ced-9(Bcl-2), ced-4(APAF1) and ced-3(Caspase) 組成了細胞凋亡的核心路徑. 這些研究指引了細胞凋亡在其他物種中的研究，並促成了包含果蠅，老鼠，人類及其他物種中類似基因的發現。線蟲中的相關研究仍有很大的發展空間；舉例而言，在線蟲所有進行細胞凋亡的細胞中，我們僅知道少數幾顆細胞啟動egl-1的機制；ced-3 的下游受質也有待補齊。若能在線蟲中建立細胞凋亡的完整藍圖，對於此領域的發展將有莫大的助益。在本研究中，我根據先前實驗的觀察結果－「grp-1這個與不對稱細胞分裂相關的基因，在同時與一些促進細胞凋亡的基因發生突變時（double mutant）會影響線蟲尾部特定細胞的命運，使其逃過死劫進而分化成為hypodermal cell導致其尾部出現特定型態上的異常。」來進行enhancer screen，在grp-1的背景下尋找促使細胞凋亡 (pro-apoptosis) 的未知基因。在本實驗中我依據線蟲尾部型態之異常分離了116個突變品系，我挑選其中71個具有較高外顯率的突變品系做進一步的分析，並依照其細胞凋亡發生的情形將其分為四群。互補試驗顯示其中6個突變是發生於已知與此機制相關的基因，包含了ced-3，ced-4以及ced-8。我目前正藉由遺傳以及性狀來分析tp6與tp7這兩個突變。這兩個突變都會導致線蟲胚胎中細胞殘骸數目的顯著減少，而其位置也暗示它們可能是此領域中未曾發現的新基因。 | zh_TW |
| dc.description.abstract | Apoptosis is an essential process for both development and homeostasis of multi-cellular animals. Previous studies of the nematode Caenorhabditis elegans have identified more than 20 genes involved in this process and placed them into a genetic pathway with four genes: egl-1(BH3-only), ced-9(Bcl-2), ced-4(APAF1) and ced-3(Caspase) that constitutes the core-cell death machinery. These works led to the finding of similar genes that control apoptosis in other organisms, including flies, mice and humans. However, there is still plenty more to be learnt; for example the mechanisms that controls egl-1’s expression in most cells doomed to die are unknown; and only few substrates of CED-3 has been found. In this study, I base on the previous observation that the double mutations in grp-1 (GTP exchange factor for ARFs, a gene involved in asymmetric cell divisions) and a pro-apoptotic gene could switch the apoptosis fate of specific cells in the tail to hypodermal cell fate and cause an arch-like morphological defect to undertake a genetic enhancer screen for new pro-apoptotic genes in the grp-1 background. From this screen, I isolated 116 mutant strains based on the “tail-defect” phenotype. Seventy one of these mutants with higher penetrance were further analyzed and put into four groups according to the pattern of their embryonic cell deaths. The complementation tests show that four mutations are alleles of previously identified pro-apoptotic genes, including ced-3,ced-4 and ced-8. I am genetically and phenotypically characterizing two mutants tp6 and tp7. They display reduced numbers of cell corpses during embryogenesis in the absence of the grp-1 mutation. On the basis of their mapping positions tp6 and tp7 likely define new pro-apoptotic genes. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-08T04:14:04Z (GMT). No. of bitstreams: 1 ntu-99-R97b43007-1.pdf: 1803310 bytes, checksum: cb9b5d4492fbd52756356ca694314a68 (MD5) Previous issue date: 2010 | en |
| dc.description.tableofcontents | Table of contents
口試委員會審定書 i 致謝 ii 中文摘要 iii Abstract iv Introduction 7 Material and Methods 15 C.elegans strains 15 Maintaining C.elegans strains 16 EMS Mutagenesis 16 Quantification of cell corpses 17 RNA interference 17 Genetic mapping and complementation test 18 Plasmid construction 19 Transgenic animals 20 Scoring the death of the tail-spike cell 20 Results 21 116 mutants were isolated from over 8000 mutagenized haploid genome 21 Seventy one of the mutants fell in to 4 distinctive classes based on the pattern of programmed cell death 21 Mutant strains no.2055, “HS0751” and”JH0054” carries mutations that are allelic to ced-8 22 tp6 and tp7 are likely mutations of novel pro-apoptotic genes 23 tp6 were predicted to be located on LGX but could also be on LGII 24 The mutated gene in strain no.2126 may be the same as of tp6 25 tp7 is located on chromosome IV near ced-3 26 dpy-24 promote programmed cell death in the tail-spike cells 26 Discussion 31 Early mapping results based on tail-defect phenotype under grp-1 RNAi 31 The identification of a novel pro-apoptotic gene 34 Filling in the gaps: Future screens 34 Reference 36 Figures 48 Figure 1 Double mutations in grp-1 and pro-apoptotic genes could switch the apoptosis fate of specific cells in the tail to hypodermal cell fate and cause an arch-like morphological defect 48 Figure 2 A brief summaries for mutagenesis and mutant isolation of this screen 49 Figure 3 A two-fold embryo showing a cell corpse 50 Figure 4 Brief summaries for generating hybrid animals used for mapping 51 Figure 5 An example of complementation test used in this study 52 Figure 6 116 mutants with the “tail-defect” with the penetrance between 20% and 100% were isolated 54 Figure 7 71 of the mutants strains selected fell into 4 distinctive classes base on the pattern of Programmed Cell Death. 55 Figure 8 The X-linkage genetic test used in this study 56 Figure 9 Genetic mapping of the mutant strain”JH0054” depending on numbers of cell corpses 57 Figure 10 Complementation test of mutations tp6, tp7 with various mutants 58 Figure 11 Genetic mapping of tp6 depending on numbers of cell corpses 61 Figure 12 Genetic mapping of tp7 depending on numbers of cell corpses 62 Figure 13 Predictions of how DRE-1 and DPY-24 regulate the cell death of the tail spike cell 64 Figure 14 Worms carrying Pcbr-ced-3::gfp under ced-3(n717) background 65 Figure 15 Worms carrying Pcbr-ced-3::gfp under ced-5(n1812) background 66 Tables 67 Table 1 Defects in PCD cause abnormal tail morphology in the grp-1 background 67 Table 2 116 mutant strains isolated and their tail-defect penetrance 68 Table 3 Programmed cell death phenotype of the 71 selected mutant strains 70 Table 4 Cell death pattern and mapping results based on tail-defect of the 16 mutant strains selected for further studies 72 Table 5 Data of mutant strain no.2326 (carrying tp6) and no.6168 (carrying tp7) and their out-crossed editions 73 Table 6 Percentage of L1 worms with visible tail-spike corpses 74 Supplemental Data 75 Figure S1 Genetic mapping of the mutation carried by mutant strain No.2055 depending on tail-defect with the usage of RNAi 75 Figure S2 Genetic mapping of the mutation carried by mutant strain No.2125 depending on tail-defect with the usage of RNAi. 77 Figure S3 Genetic mapping of the mutation carried by mutant strain No.2326 depending on tail-defect with the usage of RNAi 78 Figure S4 Genetic mapping of the mutation carried by mutant strain No.4095 depending on tail-defect with the usage of RNAi 79 Figure S5 Genetic mapping of the mutation carried by mutant strain No.4268 depending on tail-defect with the usage of RNAi 80 Figure S6 Genetic mapping of the mutation carried by mutant strain No.6168 depending on tail-defect with the usage of RNAi 81 Figure S7 Genetic mapping of the mutation carried by mutant strain No.6317 depending on tail-defect with the usage of RNAi 82 Figure S8 Genetic mapping of the mutation carried by mutant strain No.8037 depending on tail-defect with the usage of RNAi 83 Figure S9 Genetic mapping of the mutation carried by mutant strain No.8121 depending on tail-defect with the usage of RNAi 84 Figure S10 Genetic mapping of the mutation carried by mutant strain No.9298 depending on tail-defect with the usage of RNAi 85 Figure S11 Genetic mapping of the mutation carried by mutant strain No.9476 depending on tail-defect with the usage of RNAi 86 Figure S12 Genetic mapping of the mutation carried by mutant strain “HS0127” depending on tail-defect with the usage of RNAi 87 Figure S13 Genetic mapping of the mutation carried by mutant strain “HS0751” depending on tail-defect with the usage of RNAi 88 Figure S14 Genetic mapping of the mutation carried by mutant strain “JH0054” depending on tail-defect with the usage of RNAi 89 Figure S15 Genetic mapping of the mutation carried by mutant strain No.2038 depending on tail-defect with the usage of RNAi 90 Figure S16 Method of the LGII linkage test used in the study 91 Table S1 Confusing result of X-linkage test of tp6 92 Table S2 Cell death phenotypes of selected genes on LGX 93 Table S3 Mutant strain no.2126 may carry another allele of the same gene as of tp6 94 Table S4 Data of the mapping strains used in figure 11 95 Table S5 Data of the mapping strains used in figure 12 96 | |
| dc.language.iso | zh-TW | |
| dc.subject | 線蟲 | zh_TW |
| dc.subject | 誘發突變 | zh_TW |
| dc.subject | 細胞凋亡 | zh_TW |
| dc.subject | cell dath | en |
| dc.subject | apoptosis | en |
| dc.subject | enhancer screen | en |
| dc.subject | mutagenesis | en |
| dc.subject | C.elegans | en |
| dc.title | 尋找與細胞凋亡相關的新基因 | zh_TW |
| dc.title | An enhancer screen for new genes in the apoptosis pathway | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 98-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 汪宏達,陳昌熙 | |
| dc.subject.keyword | 細胞凋亡,線蟲,誘發突變, | zh_TW |
| dc.subject.keyword | apoptosis,cell dath,C.elegans,mutagenesis,enhancer screen, | en |
| dc.relation.page | 96 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2010-08-15 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 分子與細胞生物學研究所 | zh_TW |
| 顯示於系所單位： | 分子與細胞生物學研究所 | |
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